Signaling mechanisms in mirror image pain pathogenesis

. 2011 Jul ; 18 (3) : 123-7.

Status PubMed-not-MEDLINE Jazyk angličtina Země Spojené státy americké Médium print

Typ dokumentu časopisecké články, přehledy

Perzistentní odkaz   https://www.medvik.cz/link/pmid25205938

It is now clear that a peripheral nerve lesion affects contralateral non-lesioned structures, and thus such a lesion can result in mirror image pain. The pathogenesis is still not exactly known, but there are some possible signaling pathways in the contralateral reaction of the nerve tissue after unilateral nerve injury. Potential signaling pathways of contralateral changes can be generally divided into humoral and neuronal mechanisms. Damage to peripheral nerves or spinal roots produces a number of breakdown products with development of an aseptic inflammatory reaction. Released immunomodulatory cytokines are believed to be transported via blood or cerebrospinal fluid into the contralateral part of the body affecting spinal roots, dorsal root ganglia or peripheral nerves. Because neurons are elements of a highly organized network, injury to the peripheral neuron results in signals that travel transneuronally into the central nervous system and affects the contralateral homonymous neurons. There is also evidence that spinal glia creates and maintain pathological pain. Additionally, there may be compensatory changes in behavior of animals with an impact on contralateral neurons, such as altered stance and motor performance or autonomic reflex changes. Although the transneuronal signaling pathway appears to be plausible, the humoral signaling pathway or other communication systems cannot be excluded at this time. Knowledge about these processes has clinical implications for the understanding of chronic neuropathic pain states, and, therefore, further studies will be necessary. Understanding signaling mechanisms in mirror image pain pathogenesis may provide novel therapeutic targets for the management of neuropathic pain.

Zobrazit více v PubMed

Maleki J, LeBel AA, Bennett GJ et al. Patterns of spread in complex regional pain syndrome, type I (reflex sympathetic dystrophy). Pain. 2000;88(3):259–266. PubMed

Shir Y, Seltzer Z. Effects of sympathectomy in a model of causalgiform pain produced by partial sciatic nerve injury in rats. Pain. 1991;45(3):309–320. PubMed

Woda A, Pionchon P. A Unified concept of idiopathic orofacial pain: pathophysiologic features. J Orofac Pain. 2000;14(3):196–212. PubMed

Koltzenburg M, Wall PD, McMahon SB. Does the right side know what the left is doing? Trends Neurosci. 1999;22(3):122–127. PubMed

Dubovy P, Tuckova L, Jancalek R et al. Increased invasion of ED-1 positive macrophages in both ipsi- and contralateral dorsal root ganglia following unilateral nerve injuries. Neurosci Lett. 2007;427(2):88–93. PubMed

Arguis MJ, Perez J, Martinez G et al. Contralateral neuropathic pain following a surgical model of unilateral nerve injury in rats. Reg Anesth Pain Med. 2008;33(3):211–216. PubMed

Waller AW. Experiments on the section of the glossopharyngeal and hypoglossal nerves of the frog, and observations on the alterations produced thereby in the structure of their primitive fibres. Philosophical Transactions of the Royal Society of London. 1850;140:423–429.

Cheepudomwit T, Guzelsu E, Zhou C et al. Comparison of cytokine expression profile during Wallerian degeneration of myelinated and unmyelinated peripheral axons. Neurosci Lett. 2008;430(3):230–235. PubMed

Thacker MA, Clark AK, Marchand F et al. Pathophysiology of peripheral neuropathic pain: immune cells and molecules. Anesthesia and analgesia. 2007;105(3):838–847. PubMed

Schafers M, Sommer C. Anticytokine therapy in neuropathic pain management. Expert review of neurotherapeutics. 2007;7(11):1613–1627. PubMed

Ruohonen S, Jagodi M, Khademi M et al. Contralateral non-operated nerve to transected rat sciatic nerve shows increased expression of IL-1beta, TGF-beta1, TNF-alpha, and IL-10. J Neuroimmunol. 2002;132(1-2):11–17. PubMed

Petersen M, Eckert AS, Segond von Banchet G et al. Plasticity in the expression of bradykinin binding sites in sensory neurons after mechanical nerve injury. Neuroscience. 1998;83(3):949–959. PubMed

Oaklander AL, Belzberg AJ. Unilateral nerve injury down-regulates mRNA for Na+ channel SCN10A bilaterally in rat dorsal root ganglia. Brain Res Mol Brain Res. 1997;52(1):162–165. PubMed

Kleinschnitz C, Brinkhoff J, Zelenka M et al. The extent of cytokine induction in peripheral nerve lesions depends on the mode of injury and NMDA receptor signaling. J Neuroimmunol. 2004;149(1-2):77–83. PubMed

Taskinen HS, Roytta M. Increased expression of chemokines (MCP-1, MIP-1alpha, RANTES) after peripheral nerve transection. J Peripher Nerv Syst. 2000;5(2):75–81. PubMed

Kleinschnitz C, Brinkhoff J, Sommer C et al. Contralateral cytokine gene induction after peripheral nerve lesions: dependence on the mode of injury and NMDA receptor signaling. Brain Res Mol Brain Res. 2005;136(1-2):23–28. PubMed

Sommer C, Galbraith JA, Heckman HM et al. Pathology of experimental compression neuropathy producing hyperesthesia. J Neuropathol Exp Neurol. 1993;52(3):223–233. PubMed

Ek M, Engblom D, Saha S et al. Inflammatory response: pathway across the blood-brain barrier. Nature. 2001;410(6827):430–431. PubMed

Murwani R, Hodgkinson S, Armati P. Tumor necrosis factor alpha and interleukin-6 mRNA expression in neonatal Lewis rat Schwann cells and a neonatal rat Schwann cell line following interferon gamma stimulation. J Neuroimmunol. 1996;71(1-2):65–71. PubMed

Schafers M, Geis C, Brors D et al. Anterograde transport of tumor necrosis factor-alpha in the intact and injured rat sciatic nerve. J Neurosci. 2002;22(2):536–545. PubMed PMC

Hatashita S, Sekiguchi M, Kobayashi H et al. Contralateral neuropathic pain and neuropathology in dorsal root ganglion and spinal cord following hemilateral nerve injury in rats. Spine (Phila Pa 1976) 2008;33(12):1344–1351. PubMed

Sherrington CS. Flexion-reflex of the limb, crossed extension-reflex, and reflex stepping and standing. J Physiol. 1910;40(1-2):28–121. PubMed PMC

Fitzgerald M. The contralateral input to the dorsal horn of the spinal cord in the decerebrate spinal rat. Brain Res. 1982;236(2):275–287. PubMed

Fitzgerald M. Influences of contralateral nerve and skin stimulation on neurones in the substantia gelatinosa of the rat spinal cord. Neuroscience Lett. 1983;36(2):139–143. PubMed

Ritz LA, Murray CR, Foli K. Crossed and uncrossed projections to the cat sacrocaudal spinal cord: III. Axons expressing calcitonin gene-related peptide immunoreactivity. J Comp Neurol. 2001;438(4):388–398. PubMed

Suzuki H, Oyanagi K, Takahashi H et al. Evidence for transneuronal degeneration in the spinal cord in man: a quantitative investigation of neurons in the intermediate zone after long-term amputation of the unilateral upper arm. Acta neuropathol. 1995;89(5):464–470. PubMed

Arnett FC, Edworthy SM, Bloch DA et al. The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis and rheumatism. 1988;31(3):315–324. PubMed

Levine JD, Basbaum AI. Neurogenic mechanism for symmetrical arthritis. Lancet. 1990;335(8692):795. PubMed

Kidd BL, Cruwys SC, Garrett NE et al. Neurogenic influences on contralateral responses during experimental rat monoarthritis. Brain Res. 1995;688(1-2):72–76. PubMed

Donaldson LF, McQueen DS, Seckl JR. Neuropeptide gene expression and capsaicin sensitive primary afferents: maintenance and spread of adjuvant arthritis in the rat. J Physiol. 1995;486(2):473–482. PubMed PMC

Kelly S, Dunham JP, Donaldson LF. Sensory nerves have altered function contralateral to a monoarthritis and may contribute to the symmetrical spread of inflammation. Eur J Neurosci. 2007;26(4):935–942. PubMed PMC

Garrison CJ, Dougherty PM, Kajander KC et al. Staining of glial fibrillary acidic protein (GFAP) in lumbar spinal cord increases following a sciatic nerve constriction injury. Brain Res. 1991;565(1):1–7. PubMed

Hashizume H, DeLeo JA, Colburn RW et al. Spinal glial activation and cytokine expression after lumbar root injury in the rat. Spine. 2000;25(10):1206–1217. PubMed

Dennis EC. Partial peripheral nerve injury leads to activation of astroglia and microglia which parallels the development of allodynic behavior. Glia. 1998;23(1):75–83. PubMed

Ru-Rong Ji Y-RW. Neural-glial interaction in the spinal cord for the development and maintenance of nerve injury-induced neuropathic pain. Drug Dev Res. 2006;67(4):331–338.

Olsson Y. Studies on vascular permeability in peripheral nerves. I. Distribution of circulating fluorescent serum albumin in normal, crushed and sectioned rat sciatic nerve. Acta Neuropathol. 1966;7(1):1–15. PubMed

Brisby H, Olmarker K, Larsson K et al. Proinflammatory cytokines in cerebrospinal fluid and serum in patients with disc herniation and sciatica. Eur Spine J. 2002;11(1):62–66. PubMed PMC

Nguyen C, Haughton VM, Ho KC et al. Contrast enhancement in spinal nerve roots: an experimental study. Am J Neuroradiol. 1995;16(2):265–268. PubMed PMC

Skouen JS, Brisby H, Otani K et al. Protein markers in cerebrospinal fluid in experimental nerve root injury. A study of slow-onset chronic compression effects or the biochemical effects of nucleus pulposus on sacral nerve roots. Spine. 1999;24(21):2195–2200. PubMed

Cornefjord M, Nyberg F, Rosengren L et al. Cerebrospinal fluid biomarkers in experimental spinal nerve root injury. Spine. 2004;29(17):1862–1868. PubMed

Mixter WJ, Barr JS. Rupture of the intervertebral disc with involvement of the spinal canal. N Engl J Med. 1934;211:210–215.

Ahonen A, Myllyla VV, Hokkanen E. Cerebrospinal fluid protein findings in various lower back pain syndromes. Acta Neurol Scand. 1979;60:93–99. PubMed

Tunevall TG. Cerebrospinal fluid protein--an aid in the diagnosis of herniated discs. Acta Chir Scand. 1984;520:85–86. PubMed

Skouen JS, Larsen JL, Vollset SE. Cerebrospinal fluid proteins as indicators of nerve root compression in patients with sciatica caused by disc herniation. Spine. 1993;18(1):72–79. PubMed

Milligan ED, O‘Connor KA, Nguyen KT et al. Intrathecal HIV-1 envelope glycoprotein gp120 induces enhanced pain states mediated by spinal cord proinflammatory cytokines. J Neurosci. 2001;21(8):2808–2819. PubMed PMC

Brisby H, Olmarker K, Rosengren L et al. Markers of nerve tissue injury in the cerebrospinal fluid in patients with lumbar disc herniation and sciatica. Spine. 1999;24(8):742–746. PubMed

Saurwein-Teissl M, Blasko I, Zisterer K et al. An imbalance between pro- and anti-inflammatory cytokines, a characteristic feature of old age. Cytokine. 2000;12(7):1160–1161. PubMed

Bruunsgaard H, Pedersen M, Pedersen BK. Aging and proinflammatory cytokines. Curr Opin Hematol. 2001;8(3):131–136. PubMed

O‘Connor MF, Motivala SJ, Valladares EM et al. Sex differences in monocyte expression of IL-6: role of autonomic mechanisms. Am J Physiol. 2007;293(1):R145–151. PubMed

Najít záznam

Citační ukazatele

Nahrávání dat ...

Možnosti archivace

Nahrávání dat ...